Abstract: According to the present invention, Mts-1 interferes with the function of tumor suppressor p53 by binding to p53. The present inventors have demonstrated that binding of Mts-1 inhibits p53 phosphorylation by PKC, represses the DNA-binding activity of p53 and reduces the transactivation capacity of p53. The present invention has further identified that the Mts-1 protein binds to the C-terminal region of p53. Accordingly, the present invention provides compositions and methods useful for treating tumors by, e.g., intercepting the interaction between Mts-1 and p53, or inhibiting the expression or function of Mts-1.

Abstract: The present inventors have surprisingly found that the Mts-1 protein stimulates angiogenesis. In particular, the present inventors have found that Mts-1 transgenic mice developed hemangiomas and stenosis. The present inventors have also found that addition of Mts-1 proteins to the culture media increases the motility of mouse endothelial cells. Further, the present inventors have found that injection of Mts1 proteins stimulates angiogenesis in the mouse corneas. Accordingly, the present invention provides methods of enhancing angiogenesis in a subject in need thereof by administering a therapeutically effective amount of an angiogenic Mts-1 component.

Abstract: The present inventors have surprisingly found that the Mts-1 protein stimulates angiogenesis. In particular, the present inventors have found that Mts-1 transgenic mice developed hemangiomas and stenosis. The present inventors have also found that addition of Mts-1 proteins to the culture media increases the motility of mouse endothelial cells. Further, the present inventors have found that injection of Mts1 proteins stimulates angiogenesis in the mouse corneas. Accordingly, the present invention provides methods of enhancing angiogenesis in a subject in need thereof by administering a therapeutically effective amount of an angiogenic Mts-1 component.